Abstract 4363207: Targeted IL-1 Inhibition in Coxsackievirus-Induced Incessant Pericarditis: An Immunotherapy Approach

Abstract

Case Presentation: A previously healthy 33-year-old woman developed acute pericarditis with early tamponade physiology following a Coxsackievirus B infection contracted from her child. Despite urgent pericardiocentesis (550 mL) and standard anti-inflammatory therapy with NSAIDs and colchicine, she progressed to incessant pericarditis necessitating corticosteroids. Clinical Course and Timeline: Day 1: Initial presentation with tamponade physiology; Coxsackie B serology positive Days 9–10: Escalating NSAID therapy failed to control symptoms Week 2: Prednisone (30 mg/day) initiated with temporary symptom relief Week 3: Relapse during taper, resulting in rehospitalization Week 7: Recurrence despite slow taper to prednisone 5 mg Rilonacept was initiated at week 7 due to persistent steroid dependence. Within 4–6 weeks, the patient achieved complete clinical remission, normalization of inflammatory markers, and resolution of echocardiographic abnormalities. Corticosteroids were successfully discontinued over a 3-month taper while maintaining remission on rilonacept at 21-week follow-up. Discussion: This case underscores the pathophysiological relevance of IL-1β in viral pericarditis. Coxsackievirus infection induces myocardial inflammation via IL-1–mediated cytokine cascades. Traditional steroid dependence—affecting 15-30% of pericarditis patients—represents a major therapeutic challenge with significant morbidity. By acting as a soluble decoy receptor, rilonacept interrupts this pathway, offering a targeted therapeutic strategy beyond traditional broad-spectrum immunosuppression. Key Insights: 1. IL-1–mediated inflammation was a critical driver in disease persistence 2. Steroid dependence emerged despite optimal guideline-directed therapy 3. Rilonacept enabled sustained steroid-free remission Clinical Significance: IL-1 inhibition with rilonacept represents a paradigm shift in managing steroid-refractory pericarditis, especially in virally mediated cases. This case supports the growing role of biologics in cardiac inflammation and raises important questions about earlier IL-1 blockade to preempt steroid dependence. Conclusion: This case illustrates the efficacy of IL-1–targeted therapy in a complex, steroid-dependent pericarditis case and advocates for broader clinical consideration of rilonacept in viral pericarditis. Further investigation is warranted to define optimal timing and patient selection for IL-1 blockade in this setting.